PMID- 27637004
OWN - NLM
STAT- MEDLINE
DCOM- 20170223
LR  - 20220408
IS  - 1423-0097 (Electronic)
IS  - 1018-2438 (Linking)
VI  - 170
IP  - 2
DP  - 2016
TI  - A Critical Evaluation of Anti-IL-13 and Anti-IL-4 Strategies in Severe Asthma.
PG  - 122-31
LID - 10.1159/000447692 [doi]
AB  - Asthma is a high-prevalence disease, still accounting for mortality and high 
      direct and indirect costs. It is now recognized that, despite the implementation 
      of guidelines, a large proportion of cases remain not controlled. Certainly, 
      adherence to therapy and the education of patients remain the primary objective, 
      but the increasingly detailed knowledge about the pathogenic mechanisms and new 
      biotechnologies offer the opportunity to better address and treat the disease. 
      Interleukin (IL)-13 and IL-4 appear as the most suitable targets to treat the T 
      helper 2 (TH2)-mediated forms (endotypes) of asthma. IL-13 and IL-4 partly share 
      the same receptor and signaling pathways and both are deeply involved in 
      immunoglobulin E (IgE) synthesis, eosinophil activation, mucus secretion and 
      airways remodeling. Several anti-IL-13 strategies have been proposed 
      (anrukinzumab, lebrikizunab and tralokinumab), with relevant clinical results 
      reported with lebrikizumab. Such studies facilitate better definition of the 
      possible predictive markers of response to a specific treatment (e.g. 
      eosinophils, total IgE, fraction of exhaled nitric oxide and periostin). In 
      parallel, anti-IL-4 strategies have been attempted (pascolizumab, pitakinra and 
      dupilumab). So far, dupilumab was reported capable of reducing the severity of 
      asthma and the rate of exacerbations. IL-13 and IL-4 are crucial in TH2-mediated 
      inflammation in asthma, but it remains clear that only specific endotypes respond 
      to these treatments. Although the use of anti-IL-14 and anti-IL-13 strategies is 
      promising, the search for appropriate predictive biomarkers is urgently needed to 
      better apply biological treatments.
CI  - (c) 2016 S. Karger AG, Basel.
FAU - Bagnasco, Diego
AU  - Bagnasco D
AD  - Allergy and Respiratory Diseases, DIMI Department of Internal Medicine, 
      University of Genoa, IRCCS AOU San Martino-IST, Genoa, Italy.
FAU - Ferrando, Matteo
AU  - Ferrando M
FAU - Varricchi, Gilda
AU  - Varricchi G
FAU - Passalacqua, Giovanni
AU  - Passalacqua G
FAU - Canonica, Giorgio Walter
AU  - Canonica GW
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160803
PL  - Switzerland
TA  - Int Arch Allergy Immunol
JT  - International archives of allergy and immunology
JID - 9211652
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Biomarkers)
RN  - 0 (Interleukin-13)
RN  - 0 (Receptors, Interleukin-13)
RN  - 0 (Receptors, Interleukin-4)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Anti-Asthmatic Agents/pharmacology/*therapeutic use
MH  - Antibodies, Monoclonal/pharmacology/*therapeutic use
MH  - Asthma/diagnosis/*drug therapy/immunology/metabolism
MH  - Biomarkers
MH  - Humans
MH  - Interleukin-13/*antagonists & inhibitors/metabolism
MH  - Interleukin-4/*antagonists & inhibitors/metabolism
MH  - Precision Medicine
MH  - Receptors, Interleukin-13/metabolism
MH  - Receptors, Interleukin-4/metabolism
MH  - Severity of Illness Index
MH  - Signal Transduction/drug effects
MH  - T-Lymphocyte Subsets/immunology/metabolism
MH  - Th2 Cells/immunology/metabolism
EDAT- 2016/09/17 06:00
MHDA- 2017/02/24 06:00
CRDT- 2016/09/17 06:00
PHST- 2016/09/17 06:00 [entrez]
PHST- 2016/09/17 06:00 [pubmed]
PHST- 2017/02/24 06:00 [medline]
AID - 000447635 [pii]
AID - 10.1159/000447692 [doi]
PST - ppublish
SO  - Int Arch Allergy Immunol. 2016;170(2):122-31. doi: 10.1159/000447692. Epub 2016 
      Aug 3.